Abstract
Abstract Immune function is dependent on the proper development of T cells in the thymus and emigration of these cells to the periphery. We recently showed the transcription factor KLF2 is required for emigration via regulation of S1P1 (sphingosine 1-phosphate receptor 1) and CD62L in conventional αβ T cells. However, the role of KLF2 and S1P1 in trafficking of non-conventional T cell subsets (γδ T cells, Treg, NKT, and Gut intraepithelial lymphocytes -IEL) has yet to be described. We show here that KLF2 is differentially expressed within the T cells subsets studied using both mRNA expression via quantitative PCR and/or a novel KLF2-GFP reporter mouse model. While KLF2 and S1P1 can be detected in sorted non-conventional thymic T cells and Gut IEL αβ T cells, we report no detectable KLF2 in Gut IEL γδ T cells. Using several KLF2 deficient mouse models, trafficking defects were observed in Treg, NKT, and Gut-IEL (αβ and γδ) populations. Finally, the data suggest that lack of KLF2 alters both the distribution and the phenotype of γδ T cells in secondary lymphoid organs. Overall, our results suggest that KLF2 is a common means by which different T cell lineages regulate trafficking and/or entry. Funding provided by the National Institutes of Health (AI038903 to SCJ and AI039560 to KAH).
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
